Bottom Line:
Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups.These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term.Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

Affiliation: Department of Psychiatry, Chonbuk National University Medical School & Institute for Medical Sciences, Jeonju, Korea. ; Department of Psychiatry, Chonbuk National University Hospital & Research Institute of Clinical Medicine, Jeonju, Korea.

ABSTRACT

Objective: The anti-apoptotic protein Bax inhibitor-1 (BI-1) is a regulator of apoptosis linked to endoplasmic reticulum (ER) stress, and BI-1(-/-) mice exhibit increased sensitivity to tissue damage. The purpose of this study was to investigate the role of BI-1 in the pathogenesis of chronic mild stress (CMS)-induced depression-like behaviors in BI-1(-/-) mice.

Methods: We delivered CMS for 2 or 6 weeks in BI-1-knockout and wild-type mice. Control groups of BI-1-knockout and wild-type mice were left undisturbed. The measured parameters were sucrose consumption at weeks 1, 2, 3, 4, 5, and 6, spontaneous locomotion, and a forced swimming test (FST) at weeks 2 and 6.

Results: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups. Interestingly, at week 2, but not at week 6, BI-1(-/-)-stress mice showed less sucrose intake and greater immobility time than did BI-1(+/+)-stress mice.

Conclusion: These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term. Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

Mentions:
Significant differences were observed for distance traveled (F=5.121, p=0.009) and locomotor time (F=3.418, p=0.032) among the groups in the 6-week CMS treatment, but not in the 2-week CMS treatment. Post hoc analyses revealed greater distances traveled and increased locomotor time in the BI-1-/--stress group than in the BI-1+/+-control group (Table 2, Fig. 4).

Mentions:
Significant differences were observed for distance traveled (F=5.121, p=0.009) and locomotor time (F=3.418, p=0.032) among the groups in the 6-week CMS treatment, but not in the 2-week CMS treatment. Post hoc analyses revealed greater distances traveled and increased locomotor time in the BI-1-/--stress group than in the BI-1+/+-control group (Table 2, Fig. 4).

Bottom Line:
Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups.These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term.Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

Affiliation:
Department of Psychiatry, Chonbuk National University Medical School & Institute for Medical Sciences, Jeonju, Korea. ; Department of Psychiatry, Chonbuk National University Hospital & Research Institute of Clinical Medicine, Jeonju, Korea.

ABSTRACT

Objective: The anti-apoptotic protein Bax inhibitor-1 (BI-1) is a regulator of apoptosis linked to endoplasmic reticulum (ER) stress, and BI-1(-/-) mice exhibit increased sensitivity to tissue damage. The purpose of this study was to investigate the role of BI-1 in the pathogenesis of chronic mild stress (CMS)-induced depression-like behaviors in BI-1(-/-) mice.

Methods: We delivered CMS for 2 or 6 weeks in BI-1-knockout and wild-type mice. Control groups of BI-1-knockout and wild-type mice were left undisturbed. The measured parameters were sucrose consumption at weeks 1, 2, 3, 4, 5, and 6, spontaneous locomotion, and a forced swimming test (FST) at weeks 2 and 6.

Results: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups. Interestingly, at week 2, but not at week 6, BI-1(-/-)-stress mice showed less sucrose intake and greater immobility time than did BI-1(+/+)-stress mice.

Conclusion: These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term. Further study is required to deepen understanding of the role of BI-1 in protecting against depression.